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Abstract
<p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" dir="auto"
id="d3247798e117">Re-exposure to drug or drug-associated cues after withdrawal can
induce behavioral
sensitization expression in animals or increase in the expected effect to drug in
humans, which mean an enhanced drug seeking/taking motivation to trigger relapse after
abstinence. The Nucleus accumbens (NAc) is known to play a key role in mediating this
motivation. Recently, it has been shown that systemic administration of orexin receptor
1 (OXR1) antagonist attenuates animals' motivation behavior to take drug by self-administration
paradigm, which is more effectively than orexin receptor 2 (OXR2) antagonist. However,
the effect of OXR1 in the NAc on drug-induced locomotor sensitization remains elusive.
The present study was designed to investigate the effect of OXR1 in the NAc on chronic
cocaine-induced locomotor sensitization. Rats were given 10 mg/kg cocaine intraperitoneal
injection (i.p.) for five consecutive days, followed by 10 mg/kg cocaine re-exposure
(challenge) on the 14th day of withdrawal. Results showed that re-exposure to cocaine
after withdrawal could induce locomotor sensitization expression in cocaine-sensitized
rats. Simultaneously, the number of OXR1 positive neurons and OXR1 membrane protein
level in the NAc core but not the shell were significantly increased following the
cocaine re-exposure. Further, micro-infusion of SB-334867, an OXR1 selective antagonist,
into the NAc core but not the shell before cocaine re-exposure, significantly attenuated
the expression of locomotor sensitization in rats. The findings demonstrate that OXR1
in the NAc core partially mediates the expression of chronic cocaine-induced locomotor
sensitization.
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